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Editor,—I would like to make the following comments in relation to the review by Lazarus and Obuobie1:
(1) Contrary to what is stated in table 5 (possibly a typographical error), corticosteroids suppress thyroid stimulating hormone (TSH), not only in pharmacological doses,2 but also in the context of excessive endogenous cortisol secretion exemplified by Cushing's syndrome.3
(2) Among predictors of relapse after thionamide treatment of Graves' disease,1 the serum IgE concentration appears to be a promising modality, given the recent documentation of a relationship between IgE and autoantibodies against TSH receptor,4furthermore, after thionamide medication, patients with Graves' disease who have raised pretreatment IgE were significantly less likely to undergo remission (35.5% v 64.4%; p<0.002), than counterparts with normal pretreatment levels. Relapse rates (18.2% v 5.3%) tended to be higher in patients with raised pretreatment IgE but this comparison did not reach statistical significance.5 Larger studies might define these differences more accurately.
(3) Congenital hypothyroidism, to which allusion was made in the review,1 has also been the topic of recent research. A comparison of the feedback setpoint for free thyroxine modulation of serum TSH during replacement therapy in children aged <1 year compared with older counterparts showed higher prevalence of TSH resistance to thyroxine mediated feedback control (43% v10%) in the younger age group. This resistance diminished with age.6 The molecular basis for setpoint maturation will be the most exciting focus of research for decades to come.
Dr Lazarus responds:
(1) The criticism is correct and was in fact a typographical error.
(2) Although there have been data published about IgE and its role in possible prediction of relapse and remission of Graves' disease, it is not thought that there was enough substantive evidence to include this as a definitive management statement in this article.
(3) We agree that the feedback setpoint in children is of interest. However, this review was not designed to discuss the management of thyroid failure in the newborn but rather to point to advances in the appreciation of the diagnosis. Discussion of the management could be extensive and was not the aim of this review.
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